Twice-Weekly 36-Hour Intermittent Fasting Practice Attenuates Hunger, Quadruples ß-Hydroxybutyrate, and Maintains Weight Loss: A Case Report.

Intermittent fasting (IF) approach to weight loss obviates the inconvenience of calorie counting required in daily caloric restriction (DCR). A metabolic defense mechanism (MDM) obstructs weight loss and facilitates weight regain possibly by increasing hunger and efficiency of exercise energy expenditure (EEf), and by reducing resting metabolic rate (RMR) and energy expenditure (EE) including physical activity (PA). IF may test whether its paradigm can better counteract MDM than DCR. A knowledge gap exists about whether the duration of weekly uninterrupted fasts (UFs), when the IF protocols are isocaloric, affects the MDM. The aim and objective of this 82-week study were to determine whether 36 hours of near-absolute twice-weekly UF will exacerbate MDM but generate similar rates of weight and fat losses compared to four IF studies featuring 20 hours of weekly UF with both IF protocols matched for weekly hours of fast (108) and free access to food (60), a fasting-to-eating (F/E) ratio of 1.8. This case report presents results of twice-weekly fasting on non-consecutive days (5:2-NC) and compares them to results from a 4:3-NC protocol with a 20-hour UF caused by a modification of providing a 500-600 kcal meal on three fasting days (M4:3-NC). Because the large meal raises insulin concentration for four hours at the start of the fasting day, the 20-hour UF consists of the remaining eight hours on the fasting day, followed by 12 additional nocturnal hours of fasting. The hypotheses were that (1) because of their matched F/E ratio, the rates of weight and fat losses will be similar in both protocols, and (2) because of its longer UF period, hunger will be higher and RMR and EE will be lower, in 5:2-NC than in M4:3-NC protocol. The main findings were that the 5:2-NC protocol produced (1) slower rates of weight and fat losses, (2) modest reduction in the sensation of hunger and substantial decline in fullness, (3) no change in RMR and EE, and (4) fourfold post-fast increase in the circulating concentration of the ketone body ß-hydroxybutyrate (BHB), 2.5 greater than in the M4:3-NC protocol. The absence of increased hunger and changes in EE, the variability of the rate of weight loss in the 5:2-NC protocol, plus increased EEf in one M4:3-NC study, suggest that IF does not mitigate MDM, but that shortened UF period in M4:3-NC reduces the rise in BHB. Thus, the addition of a large meal on fasting days is unnecessary for the prevention of hunger and is counterproductive for increases in BHB and its potential health benefits. Continuous practice of the 5:2-NC protocol allows sustained weight loss and maintenance of lost weight with diminished hunger for as long as it is implemented.

How to Suppress Mineral Loss and Stimulate Anabolism in Postmenopausal Bones with Appropriate Timing of Exercise and Nutrients.

Background. Bone Health and Osteoporosis Foundation (BHOF) reports that as of 2023, approximately 10 million of older Americans have osteoporosis and another 44 million have low bone density. Osteoporosis is a serious handicap for the elderly and, in particular, for estrogen-deficient postmenopausal women, as it increases the risk of debilitating bone weakness and fractures. The BHOF recommendations for prevention of osteopenia, osteoporosis and bone fractures are to perform weight-bearing and muscle-strengthening exercises and to take recommended amounts of daily calcium and vitamin D. Methods. The purpose of this review is to describe and discuss recent evidence-based research on how to effectively utilize timing of exercise and calorie intake for stimulation of postmenopausal bone anabolism, and to provide this new information in the form of specific and actionable recommendations. Results. The five evidence-based recommendations are as follows: 1. Select an appropriate circadian time of day for exercise; 2. Increase walking speed to raise the movement momentum; 3. Eat a weight-maintenance meal one or two hours before the exercise bout; 4. Sustain the duration of walking activity (impulse) for 40 to 45 min; and 5. Repeat effective exercise stimulus 7 to 8 h after the first one to double the anabolic effect. Osteogenesis can also be increased with subthreshold mechanical loading, where needed, under several special circumstances. Conclusions. This review should provide pragmatic actionable pointers on how to utilize the idiosyncratic bone responsiveness to timing of movement and meals to prevent osteoporosis and encourage research toward a better understanding of how bone detects adequacy of a mechanical stimulus and determines duration of necessary rest to recover its sensitivity to mechanical stimulation and nutrients.

Are gastrointestinal signals the principal guides to human appetite and energy balance?

In view of the exponential rise of global obesity in the past three quarters of the century, it is useful to examine what is driving this change and what approaches can curb it. The chief drivers of weight gain are, on one hand our misunderstanding of the mechanisms controlling energy balance, and, on the other, reliance on current, potentially misleading conflicting scientific opinions and government policies regarding the controls of human appetite. This review outlines the evidence that: (1) there is no direct bioenergetic feedback from energy metabolism or energy stores to the brain mechanisms guiding feeding and energy expenditure, (2) human appetite is controlled by signals originating from an empty or full stomach, food palatability and opportunities to eat as well by the rate of food absorption, that (3) humans bear a genetic burden of having high ability and capacity to store fat and mechanisms that curb body- mass and fat loss, (4) humans are motivated to overconsume while maintaining low energy expenditure, and (5) commercial interests of food businesses marketing highly palatable foods, and wide-spread mechanization of living tasks and urban design reduce the need for physical work and movement. The non-pharmacological and non-surgical solutions to obesity involve an understanding of human genetic impediments and environmental obstacles to maintaining healthy weight, coupled with deliberate corrective or preventive behaviors, such as understanding and using gastrointestinal tract signals that provide sufficient, albeit subtle, cues for sensible food intake, and using daily weight monitoring and activity tracking devices to record and motivate healthy levels of physical activity.

Effects of Walking Speed on Total and Regional Body Fat in Healthy Postmenopausal Women.

INTRODUCTION: This study had two aims: (1) To confirm the efficacy of exercise speed and impulse (session duration at a given speed) to produce total and abdominal fat loss in postmenopausal women, and (2) compare the exercise speed and impulse necessary for the stimulation of fat loss to the suppression of bone mineral loss. Of special interest was to compare these parameters of exercise on fat loss in the same study and with the same subjects where they were found to suppress bone mineral loss. We hypothesized that (1) more total fat will be lost with slow walking and a longer impulse than with fast speed and shorter impulse, and (2) more abdominal subcutaneous (SC) and visceral fat (VF) will be lost with fast walking speed. MATERIALS AND METHODS: Fat loss and suppression of bone mineral loss were measured in the same 25 subjects after 15 weeks, and fat measurements were also taken after 30 weeks in 16 residual subjects. Study parameters were walking a 4.8 km distance 4 days/week at either 6.6 km/h (120% of ventilatory threshold (VT)) or at 5.5 km/h (101.6% of VT) and expending 300 kcal/session. Body composition (fat and lean body mass, LBM) was measured with dual-energy X-ray absorptiometry (DXA) and anthropometric methods. RESULTS: Slow walkers in the residual group progressively lost a significant percent of total body fat over 30 weeks while no such loss occurred after 15 weeks in fast walkers in either group, supporting hypothesis 1. However, the 20% higher starting body fat in 16 residual slow relative to fast subjects suggests that exercise fat loss is greater in overweight than in lean subjects. In fast walkers, fat loss occurred after 30 weeks of training. Hypothesis 2 was not supported as both speeds led to equal VF loss in 30-week group as estimated by waist circumference (CF) confirming that VF responds to the magnitude of energy expenditure and not the walking speed. CONCLUSIONS: Total body fat is lost through walking at all speeds, but the change is more rapid, clear, and initially greater with slow walking in overweight subjects. A longer exercise impulse at a lower speed in our study initially produced greater total fat loss than a shorter one with fast walking speed. This was reversed in comparison to how the same exercise in the same subjects suppressed bone mineral loss. Data from other studies indicate that longer impulses may promote greater fat loss at both slow and high exercise speeds, and our study providing only a 4.8 km walking distance may have limited the walking impulse and the magnitude of fat loss. Increased exercise energy expenditure at either walking speed produces equivalent declines in visceral fat in postmenopausal women, and with sufficiently long impulses, should reduce disabilities associated with central obesity.

Timing of Meals and Exercise Affects Hormonal Control of Glucoregulation, Insulin Resistance, Substrate Metabolism, and Gastrointestinal Hormones, but Has Little Effect on Appetite in Postmenopausal Women.

The current prevalence of obesity in the US is strongly associated with excessive food intake and insufficient physical activity. This study examined whether changing the timing of exercise before or after two daily meals could alter human appetite for food. Fifty-four healthy postmenopausal women were matched by body weight and assigned to two groups: (1) two bouts of 2-h moderate-intensity exercise ending one hour before each weight-maintenance meal (XM, n = 23), (2) two-hour moderate-intensity exercise starting 1 h after each weight-maintenance meal (MX, n = 23), and one sedentary control (SED) arm (n = 8). Measurements included appetite ratings, circulating glucose, free fatty acids (FFAs), a ketone body D-ß-hydroxybutyrate (BHB), glucoregulatory hormones insulin and glucagon, and gastrointestinal hormones associated with food digestion and absorption and implicated in appetite sensations. XM group increased concentrations of FFAs and BHB during exercise and increased insulin and homeostatic assessment of insulin resistance (HOMA-IR) during postprandial periods. MX group reduced postprandial insulin and HOMA-IR by about 50% without a major change in plasma glucose. There was brief suppression of hunger and an increase in satiation in both exercise groups near the end of the first postprandial period. The time course of hunger was unrelated to the perturbations in fuel metabolism, depletion of liver glycogen, and not correlated with concentration changes in hunger-stimulating hormone ghrelin during XM exercise before meals. Similarly, there was no correlation between the time course of fullness during exercise after meals with the postprandial secretion of gastrointestinal hormones including cholecystokinin (CCK) that has been linked to satiation. Hunger and satiation appear to depend on oral intake and gastrointestinal processing of nutrients and are not affected by metabolic and hormonal consequences of the timing of exercise with respect to meals. Moderate-intensity exercise performed shortly after meals induces a rapid and highly effective lowering of insulin resistance.

Anabolic Bone Stimulus Requires a Pre-Exercise Meal and 45-Minute Walking Impulse of Suprathreshold Speed-Enhanced Momentum to Prevent or Mitigate Postmenopausal Osteoporosis within Circadian Constraints.

Osteoporosis currently afflicts 8 million postmenopausal women in the US, increasing the risk of bone fractures and morbidity, and reducing overall quality of life. We sought to define moderate exercise protocols that can prevent postmenopausal osteoporosis. Our previous findings singled out higher walking speed and pre-exercise meals as necessary for suppression of bone resorption and increasing of markers of bone formation. Since both studies were amenable to alternate biomechanical, nutritional, and circadian interpretations, we sought to determine the relative importance of higher speed, momentum, speed-enhanced load, duration of impulse, and meal timing on osteogenic response. We hypothesized that: (1) 20 min of exercise one hour after eating is sufficient to suppress bone resorption as much as a 40-min impulse and that two 20 min exercise bouts separated by 7 h would double the anabolic effect; (2) early morning exercise performed after eating will be as effective as mid-day exercise for anabolic outcome; and (3) the 08:00 h 40-min. exercise uphill would be as osteogenic as the 40-min exercise downhill. Healthy postmenopausal women, 8 each, were assigned to a no-exercise condition (SED) or to 40- or 20-min exercise bouts, spaced 7 h apart, for walking uphill (40 Up and 20 Up) or downhill (40 Down and 20 Down) to produce differences in biomechanical variables. Exercise was initiated at 08:00 h one hour after eating in 40-min groups, and also 7 h later, two hours after the midday meal, in 20-min groups. Measurements were made of CICP (c-terminal peptide of type I collagen), osteocalcin (OC), and bone-specific alkaline phosphatase (BALP), markers of bone formation, and of the bone resorptive marker CTX (c-terminal telopeptide of type 1 collagen). The osteogenic ratios CICP/CTX, OC/CTX, and BALP/CTX were calculated. Only the 40-min downhill exercise of suprathreshold speed-enhanced momentum, increased the three osteogenic ratios, demonstrating the necessity of a 40-min, and inadequacy of a 20-min, exercise impulse. The failure of anabolic outcome in 40-min uphill exercise was attributed to a sustained elevation of PTH concentration, as its high morning elevation enhances the CTX circadian rhythm. We conclude that postmenopausal osteoporosis can be prevented or mitigated in sedentary women by 45 min of morning exercise of suprathreshold speed-enhanced increased momentum performed shortly after a meal while walking on level ground, or by 40-min downhill, but not 40-min uphill, exercise to avoid circadian PTH oversecretion. The principal stimulus for the anabolic effect is exercise, but the prerequisite for a pre-exercise meal demonstrates the requirement for nutrient facilitation.

Why We Eat Too Much, Have an Easier Time Gaining Than Losing Weight, and Expend Too Little Energy: Suggestions for Counteracting or Mitigating These Problems.

The intent of this review is to survey physiological, psychological, and societal obstacles to the control of eating and body weight maintenance and offer some evidence-based solutions. Physiological obstacles are genetic and therefore not amenable to direct abatement. They include an absence of feedback control against gaining weight; a non-homeostatic relationship between motivations to be physically active and weight gain; dependence of hunger and satiation on the volume of food ingested by mouth and processed by the gastrointestinal tract and not on circulating metabolites and putative hunger or satiation hormones. Further, stomach size increases from overeating and binging, and there is difficulty in maintaining weight reductions due to a decline in resting metabolism, increased hunger, and enhanced efficiency of energy storage. Finally, we bear the evolutionary burden of extraordinary human capacity to store body fat. Of the psychological barriers, human craving for palatable food, tendency to overeat in company of others, and gullibility to overeat when offered large portions, can be overcome consciously. The tendency to eat an unnecessary number of meals during the wakeful period can be mitigated by time-restricted feeding to a 6-10 hour period. Social barriers of replacing individual physical work by labor-saving appliances, designing built environments more suitable for car than active transportation; government food macronutrient advice that increases insulin resistance; overabundance of inexpensive food; and profit-driven efforts by the food industry to market energy-dense and nutritionally compromised food are best overcome by informed individual macronutrient choices and appropriate timing of exercise with respect to meals, both of which can decrease insulin resistance. The best defense against overeating, weight gain, and inactivity is the understanding of factors eliciting them and of strategies that can avoid and mitigate them.

Nutrient Intake Prior to Exercise Is Necessary for Increased Osteogenic Marker Response in Diabetic Postmenopausal Women.

Type 2 diabetes increases bone fracture risk in postmenopausal women. Usual treatment with anti-resorptive bisphosphonate drugs has some undesirable side effects, which justified our interest in the osteogenic potential of nutrition and exercise. Since meal eating reduces bone resorption, downhill locomotion increases mechanical stress, and brief osteogenic responsiveness to mechanical stress is followed by several hours of refractoriness, we designed a study where 40-min of mechanical stress was manipulated by treadmill walking uphill or downhill. Exercise preceded or followed two daily meals by one hour, and the meals and exercise bouts were 7 hours apart. Fifteen subjects each performed two of five trials: No exercise (SED), uphill exercise before (UBM) or after meals (UAM), and downhill exercise before (DBM) or after meals (DAM). Relative to SED trial, osteogenic response, defined as the ratio of osteogenic C-terminal propeptide of type I collagen (CICP) over bone-resorptive C-terminal telopeptide of type-I collagen (CTX) markers, increased in exercise-after-meal trials, but not in exercise-before-meal trials. CICP/CTX response rose significantly after the first exercise-after-meal bout in DAM, and after the second one in UAM, due to a greater CICP rise, and not a decline in CTX. Post-meal exercise, but not the pre-meal exercise, also significantly lowered serum insulin response and homeostatic model (HOMA-IR) assessment of insulin resistance.

Understanding Human Physiological Limitations and Societal Pressures in Favor of Overeating Helps to Avoid Obesity.

Fat gain in our United States (US) environment of over-abundant, convenient, and palatable food is associated with hypertension, cardiovascular disease, diabetes, and increased mortality. Fuller understanding of physiological and environmental challenges to healthy weight maintenance could help prevent these morbidities. Human physiological limitations that permit development of obesity include a predilection to overeat palatable diets, inability to directly detect energy eaten or expended, a large capacity for fat storage, and the difficulty of losing body fat. Innate defenses resisting fat loss include reduced resting metabolism, increased hunger, and high insulin sensitivity, promoting a regain of fat, glycogen, and lean mass. Environmental challenges include readily available and heavily advertised palatable foods, policies and practices that make them abundant, less-than-ideal recommendations regarding national dietary macronutrient intake, and a frequently sedentary lifestyle. After gaining excess fat, some metabolic burdens can be mitigated though thoughtful selection of nutrients. Reduced dietary salt helps lower hypertension, less dietary sugar lowers risk of cardiovascular disease and obesity, and reducing proportion of dietary carbohydrates lowers post-meal insulin secretion and insulin resistance. Food intake and exercise should also be considered thoughtfully, as exercise in a fasted state and before the meals raises glucose intolerance, while exercising shortly after eating lowers it. In summary, we cannot directly detect energy eaten or expended, we have a genetic predisposition to eat palatable diets even when not hungry, and we have a large capacity for fat storage and a difficult time permanently losing excess fat. Understanding this empowers individuals to avoid overeating and helps them avoid obesity.

Third Exposure to a Reduced Carbohydrate Meal Lowers Evening Postprandial Insulin and GIP Responses and HOMA-IR Estimate of Insulin Resistance.

BACKGROUND: Postprandial hyperinsulinemia, hyperglycemia, and insulin resistance increase the risk of type 2 diabetes (T2D) and cardiovascular disease mortality. Postprandial hyperinsulinemia and hyperglycemia also occur in metabolically healthy subjects consuming high-carbohydrate diets particularly after evening meals and when carbohydrate loads follow acute exercise. We hypothesized the involvement of dietary carbohydrate load, especially when timed after exercise, and mediation by the glucose-dependent insulinotropic peptide (GIP) in this phenomenon, as this incretin promotes insulin secretion after carbohydrate intake in insulin-sensitive, but not in insulin-resistant states. METHODS: Four groups of eight metabolically healthy weight-matched postmenopausal women were provided with three isocaloric meals (a pre-trial meal and two meals during the trial day) containing either 30% or 60% carbohydrate, with and without two-hours of moderate-intensity exercise before the last two meals. Plasma glucose, insulin, glucagon, GIP, glucagon-like peptide 1 (GLP-1), free fatty acids (FFAs), and D-3-hydroxybutyrate concentrations were measured during 4-h postprandial periods and 3-h exercise periods, and their areas under the curve (AUCs) were analyzed by mixed-model ANOVA, and insulin resistance during fasting and meal tolerance tests within each diet was estimated using homeostasis-model assessment (HOMA-IR). RESULTS: The third low-carbohydrate meal, but not the high-carbohydrate meal, reduced: (1) evening insulin AUC by 39% without exercise and by 31% after exercise; (2) GIP AUC by 48% without exercise and by 45% after exercise, and (3) evening insulin resistance by 37% without exercise and by 24% after exercise. Pre-meal exercise did not alter insulin-, GIP- and HOMA-IR- lowering effects of low-carbohydrate diet, but exacerbated evening hyperglycemia. CONCLUSIONS: Evening postprandial insulin and GIP responses and insulin resistance declined by over 30% after three meals that limited daily carbohydrate intake to 30% compared to no such changes after three 60%-carbohydrate meals, an effect that was independent of pre-meal exercise. The parallel timing and magnitude of postprandial insulin and GIP changes suggest their dependence on a delayed intestinal adaptation to a low-carbohydrate diet. Pre-meal exercise exacerbated glucose intolerance with both diets most likely due to impairment of insulin signaling by pre-meal elevation of FFAs.

Associations of objectively assessed sleep and physical activity in 11-year old children.

AIM: Objective methods were used to evaluate children's sleep and physical activity over several days in order to test the hypotheses that: (1) low average sleep duration and/or sleep efficiency are linked to a low amount of physical activity; and (2) a reduction in sleep quantity and/or sleep efficiency during the night is followed by a decrease in physical activity the following day. METHODS: This is a multi-centre, observational study involving 276 children, aged 10.5-12 years, from diverse urban settings in Croatia, Slovenia and the US. Sleep and activity were monitored for 2-6 days (median = 4) using the Sensewear Armband™ multi-sensor body monitor. RESULTS: While average sleep duration and efficiency were unrelated to physical activity, within-subjects associations revealed that an extra hour spent in bed during the night was followed by a 16-minute decrease in moderate-to-vigorous physical activity (p < 0.001). This was accompanied by a 4.5 kJ/kg and 5.9 kJ/kg lower total daily energy expenditure in boys and girls, respectively (p < 0.001). CONCLUSIONS: This study found no evidence for a link between short sleep and low or reduced physical activity.

Counterregulation of insulin by leptin as key component of autonomic regulation of body weight.

A re-examination of the mechanism controlling eating, locomotion, and metabolism prompts formulation of a new explanatory model containing five features: a coordinating joint role of the (1) autonomic nervous system (ANS); (2) the suprachiasmatic (SCN) master clock in counterbalancing parasympathetic digestive and absorptive functions and feeding with sympathetic locomotor and thermogenic energy expenditure within a circadian framework; (3) interaction of the ANS/SCN command with brain substrates of reward encompassing dopaminergic projections to ventral striatum and limbic and cortical forebrain. These drive the nonhomeostatic feeding and locomotor motivated behaviors in interaction with circulating ghrelin and lateral hypothalamic neurons signaling through melanin concentrating hormone and orexin-hypocretin peptides; (4) counterregulation of insulin by leptin of both gastric and adipose tissue origin through: potentiation by leptin of cholecystokinin-mediated satiation, inhibition of insulin secretion, suppression of insulin lipogenesis by leptin lipolysis, and modulation of peripheral tissue and brain sensitivity to insulin action. Thus weight-loss induced hypoleptimia raises insulin sensitivity and promotes its parasympathetic anabolic actions while obesity-induced hyperleptinemia supresses insulin lipogenic action; and (5) inhibition by leptin of bone mineral accrual suggesting that leptin may contribute to the maintenance of stability of skeletal, lean-body, as well as adipose tissue masses.

Circadian and ultradian components of hunger in human non-homeostatic meal-to-meal eating.

UNLABELLED: A unifying physiological explanation of the urge to initiate eating is still not available as human hunger in meal-to-meal eating may not be under homeostatic control. We hypothesized that a central circadian and a gastrointestinal ultradian timing mechanism coordinate non-deprivation meal-to-meal eating. We examined hunger as a function of time of day, inter-meal (IM) energy expenditure (EE), and concentrations of proposed hunger-controlling hormones ghrelin, leptin, and insulin. METHODS: In two crossover studies, 10 postmenopausal women, BMI 23-26 kg/m(2) engaged in exercise (EX) and sedentary (SED) trials. Weight maintenance meals were provided at 6h intervals with an ad libitum meal at 13 h in study 1 and 21 h snack in study 2. EE during IM intervals was measured by indirect calorimetry and included EX EE of 801 kcal in study 1, and 766-1,051 kcal in study 2. Hunger was assessed with a visual analog scale and blood was collected for hormonal determination. RESULTS: Hunger displayed a circadian variation with acrophase at 13 and 19 h and was unrelated to preceding EE. Hunger was suppressed by EX between 10 and 16 h and bore no relationship to either EE during preceding IM intervals or changes in leptin, insulin, and ghrelin; however leptin reflected IM energy changes and ghrelin and insulin, prandial events. CONCLUSIONS: During non-deprivation meal-to-meal eating, hunger appears to be under non-homeostatic central circadian control as it is unrelated to EE preceding meals or concentrations of proposed appetite-controlling hormones. Gastrointestinal meal processing appears to intermittently suppress this control and entrain an ultradian hunger pattern.

Effect of endurance exercise on resting testosterone levels in sedentary subjects.

OBJECTIVE: To investigate the effects of moderate-intensity and low frequency exercise on resting serum testosterone and cortisol levels, resting heart rate, and isokinetic strength among healthy sedentary young men. DESIGN: A randomized controlled study. Forty sedentary young men aged 18 to 25 years old, pedaled 50 minutes on a bicycle ergometry at 60% of maximal effort once a week for 12 weeks in an exercise group. OUTCOME MEASURES: Resting total and free serum testosterone, serum cortisol, anthropometric data, resting heart rate, and isokinetic strength during shoulder and knee extensions. RESULTS: Resting serum total and free testosterone, as well as cortisol did not differ significantly between groups. Neither group showed any significant changes in anthropometric data and isokinetic strength at the end of study. However, the resting heart rate of the exercise group reduced significantly after the training (p < 0.05). Also, the isokinetic strength of shoulder and knee significantly increased (p < 0.05). CONCLUSIONS: Twelve weeks of moderate-intensity and low frequency training had no effect on resting serum testosterone, but were sufficient to increase aerobic fitness among sedentary young men. The type of exercise training may encourage sedentary individuals to participate regularly in the program on physical activity.

Effect of once a week endurance exercise on fitness status in sedentary subjects.

OBJECTIVE: To study whether 3-months aerobic exercise training at moderate intensity once a week can increase fitness status in healthy sedentary young men. MATERIAL AND METHOD: Randomized controlled study was performed in 37 sedentary young men, 18 to 25 years old. The exercise group (19) was assigned to work on bicycle ergometry at 60% of maximal effort, once a week for 12 weeks. The control group (18) lived a normal life style. Before and after training, aerobic fitness (VO2(max)), resting heart rate, lipid profile, and isokinetic power and strength of shoulder and knee were evaluated. RESULTS: In the exercise group, there was a significant increase in most fitness parameters compared with control, VO2(max) (19.7%), isokinetic power and strength of shoulder and knee (14.9%), and resting heart rate decreased (7.4%). CONCLUSION: Moderate-intensity training once a week for at least 12 weeks was sufficient to increase aerobic fitness in sedentary young men. This low frequency of exercise training may be used to encourage sedentary individuals for more compliance with physical activity.

Nonhomeostatic control of human appetite and physical activity in regulation of energy balance.

Ghrelin and leptin, putative controllers of human appetite, have no effect on human meal-to-meal appetite but respond to variations in energy availability. Nonhomeostatic characteristics of appetite and spontaneous activity stem from inhibition by leptin and ghrelin of brain reward circuit that is responsive to energy deficit, but refractory in obesity, and from the operation of a meal-timing circadian clock.

Two bouts of exercise before meals, but not after meals, lower fasting blood glucose.

INTRODUCTION: Reduced counterregulatory responses to a next-day hypoglycemic challenge and hypoglycemia result from two spaced episodes of moderate-intensity exercise and have been characterized as exercise-associated autonomic failure. We hypothesized that this phenomenon is caused by postabsorptive state at the time of exercise rather than by autonomic failure. METHODS: Participants were nine healthy postmenopausal women in a crossover study. Two hours of treadmill exercise at 43% of maximal effort were performed twice a day, separated by 5 h, either 1 h before (Before-Meals trial) or 1 h after a meal (After-Meals trial). Plasma insulin, counterregulatory hormones (glucagon, growth hormone, cortisol), and metabolites (glucose, free fatty acids, ketones) were measured to evaluate the effects of nutritional timing. Analyses of HR and vagal tone were measured to assess autonomic function. RESULTS: Before-Meals exercise, but not After-Meals exercise, reduced postabsorptive plasma glucose by 20.2% during a 16-h period, without a change in counterregulatory response, and elicited postexercise ketosis. A 49% increase in insulin-glucagon ratio during meals, a 1 mM decline in glucagon glycemic threshold, and a reduced vagal tone during exercise were associated with Before-Meals but not with After-Meals trials. CONCLUSIONS: These results demonstrate that exercise performed in postabsorptive, but not in postprandial state, lowers glucoregulatory set point and glucagon glycemic threshold and is accompanied by reduced vagal tone, counterregulatory responses, and glucagon glycemic threshold and by increased insulin-glucagon ratio. Reduced counterregulatory response, altered neuroendocrine function, and sustained lowering of blood glucose are most likely the consequences of reduced carbohydrate availability during exercise.

Appetite responds to changes in meal content, whereas ghrelin, leptin, and insulin track changes in energy availability.

CONTEXT: It is uncertain how between-meal variations in energy availability and physiological changes in ghrelin, leptin, and insulin affect appetite. OBJECTIVE: The aim of the study was to examine the influence on human appetite of the meal size and its nutrient content or changes in energy availability and concentrations of ghrelin, leptin, and insulin. DESIGN: We conducted a crossover study manipulating meal size and energy availability through exercise energy expenditure and iv nutrient replacement (TPN). SETTING: The study was performed at a Clinical Research Center. PARTICIPANTS: Ten healthy postmenopausal women (age, 59.7 +/- 1.5 yr; mean body mass index, 26 kg/m(2)) were studied. INTERVENTIONS: We conducted trials based on different morning meal size (418 vs. 2090 KJ), presence or absence of exercise energy expenditure (2273 to 2361 KJ), energy replacement by TPN (1521 to 1538 KJ), and a midday ad libitum meal. MAIN OUTCOME MEASURES: Changes in hunger, fullness, midday ad libitum food consumption, and concentrations of ghrelin, leptin, insulin, and metabolic fuels were measured. We also performed midday meal tests for the presence of caloric compensation. RESULTS: Appetite was influenced by the size and energy content of the meals, but not by variation in energy availability which also did not trigger consummatory compensation. Exercise reduced hunger and increased fullness. Ghrelin, leptin, and insulin responded to changes in energy availability but not to meal size. Appetite was unaffected by physiological changes in ghrelin, leptin, or insulin. CONCLUSIONS: During rest, appetite is influenced by the size and energy content of meals, but it bears no homeostatic relationship to between-meal changes in energy availability due to small meals, exercise, or TPN, or concentrations of ghrelin, leptin, and insulin.

Walking intensity for postmenopausal bone mineral preservation and accrual.

INTRODUCTION: Mechanical stresses on the bone are an important aspect of physical activity that promotes bone preservation and increases in bone mass. Exercise intensities leading to bone preservation and accrual have not been adequately defined for humans in general, and postmenopausal women in particular. MATERIALS AND METHODS: To quantify parameters of effective walking intensity for preservation and accrual of bone mineral, healthy postmenopausal women engaged in 30 weeks of supervised walking, 4.8 km per day, 4 days a week at intensities of 102% or 123% of the ventilatory threshold (VT) equivalent to 67% and 86% of maximal effort (VO2 max). Subjects were matched by age, body mass, hormone replacement status (HRT) and VT. Areal bone mineral density (aBMD) determined by DXA (n=25) and bone formation markers osteocalcin (OC), and bone-specific alkaline phosphatase (bALP) (n=43), were measured at the outset and at 15-week intervals. Peak vertical forces at corresponding intensities were measured (n=9) on a force plate. RESULTS: aBMD of legs and whole body, but not of other sites, and lean mass of legs, but not of arms, increased after 15 weeks of high intensity, compared to moderate losses for low intensity training. Leg and total body aBMD was preserved and slightly increased with loads greater than 872.3 newtons (N) with a walking intensity above 115% of VT or 74% of VO2 max, speeds above 6.14 km/h, and heart rates above 82.3% of age-specific maximum. OC and bALP did not correlate with training-induced changes in aBMD. CONCLUSIONS: At exercise intensities above 115% of VT or 74% of VO2 max, and walking speeds above 6.14 km/h, mechanical loading of 872.3 N or 1.22 times body weight is sufficient for increases in leg muscle mass and preservation of BMD in postmenopausal women.